Activation of c-Myc is one of the most common oncogenic events in human malignancies [1, 2]. In normal cells, the Myc family of transcription factors (c-Myc, L-Myc, and N-Myc) regulates a diverse set of biological processes including DNA replication, gene transcription, and protein translation. Consequently, numerous cellular processes are regulated by Myc, including growth, proliferation, apoptosis, metabolism, differentiation, self-renewal, and angiogenesis [3, 4, 5]. It has been estimated that c-Myc regulates expression of more than 15% of all genes and therefore is considered to be a master regulator [6]. In malignant cells, Myc activation can occur through several mechanisms such as point mutation, somatic gene amplification, chromosomal translocation, overexpression, enhanced translation, and increased protein stability [2]. One estimate attributes 100,000 cancer deaths annually in the United States to deregulation of Myc [6]. Burkitt's lymphoma provides a paradigm for Myc deregulation in malignancy as nearly all cases involve balanced translocation of the MYC gene and overexpression of the oncoprotein [7, 8]. c-Myc deregulation may result in uncontrolled cell proliferation, alterations in the apoptotic pathway, genomic instability, escape from immune surveillance, growth factor independence, and immortalization [2]. The report that the inhibition of Myc in vivo eradicated lung cancer in mice [9] shows the potential of Myc as a target in cancer treatment.